Protocol for engineering and validating a synthetic mitochondrial intermembrane bridge in mammalian cells

Review Multidisciplinary Sciences

Mitochondria shed their outer membrane in response to infection-induced stress

Xianhe Li et al.

Summary: During Toxoplasma gondii infection in mammalian cells, large SPOTs (structures positive for OMM) form and mediate the depletion of OMM proteins mitofusin 1 and 2, thereby restricting parasite growth. The formation of SPOTs depends on the parasite effector TgMAF1 and the host mitochondrial import receptor TOM70.

SCIENCE (2022)

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Article Multidisciplinary Sciences

Protease OMA1 modulates mitochondrial bioenergetics and ultrastructure through dynamic association with MICOS complex

Martonio Ponte Viana et al.

Summary: Remodeling of mitochondrial ultrastructure is critical for organelle physiology and apoptosis. OMA1, in addition to its role in mitochondrial division, is also required for maintaining intermembrane connectivity by dynamically associating with MICOS. This OMA1-MICOS relay is crucial for optimal bioenergetic output and cell apoptosis. Loss of OMA1 affects these functions but can be alleviated by a MICOS-emulating intermembrane bridge, highlighting OMA1's essential role in mitochondrial physiology.

ISCIENCE (2021)

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Article Cell Biology